文献类型：期刊文献

中文题名：当归对阴虚哮喘BALB/c小鼠Th2优势免疫应答的影响

英文题名：Effects of Angelicae Sinensis Radix on Th2 Dominant Immune Response in Asthmatic BALB/c Mice with Yin Deficiency Syndrome

作者：程小丽[1];李荣科[1];王志旺[1];任远[1];妥海燕[1];刘雪枫[1]

第一作者：程小丽

机构：[1]甘肃中医药大学

第一机构：甘肃中医药大学

年份：2016

卷号：33

期号：3

起止页码：272

中文期刊名：中国现代应用药学

外文期刊名：Chinese Journal of Modern Applied Pharmacy

收录：CSTPCD;;CSCD:【CSCD_E2015_2016】；

基金：国家自然科学基金(81460668);甘肃省自然科学基金(1310RJZA086)

语种：中文

中文关键词：当归;阴虚哮喘;BALB/c小鼠;Th2优势免疫应答

外文关键词：Angelicae Sinensis Radix; asthma with Yin deficiency syndrome; BALB/c mouse; Th2 dominant immune response

摘要：目的探讨当归对阴虚哮喘BALB/c小鼠Th2细胞优势免疫应答的影响。方法采用注射卵清白蛋白(ovalbumin,OVA)致敏、吸入OVA激发的方法来复制BALB/c小鼠哮喘模型,实验后期给予甲状腺素以复制阴虚哮喘模型,通过观测哮喘行为学、血清及支气管肺泡灌洗液(broncho-alveolar lavage fluid,BALF)中IL-4、IL-13的水平、BALF及肺组织中炎性细胞的含量、肺组织中GATA-3蛋白表达水平,探讨当归的平喘作用及对Th2细胞优势免疫应答的影响。结果当归可明显减少阴虚哮喘小鼠哮喘发作的次数及其发作时的症状,改善肺组织病理学而减少肺组织及BALF中炎性细胞的数量,降低血清及BALF中IL-4、IL-13的水平,抑制肺组织中GATA-3蛋白的表达(P<0.05或0.01);同时,当归与地塞米松配伍后对嗜酸粒细胞、IL-4及GATA-3的抑制作用具有一定的协同作用(P<0.05或0.01)。结论当归具有平喘作用,抑制细胞因子IL-4、IL-13及转录因子GATA-3的表达而缓解Th2优势免疫应答可能是其作用机制之一。
OBJECTIVE To study the effects of Angelicae Sinensis Radix on Th2 dominant immune response in asthmatic BALB/c mice with Yin deficiency syndrome. METHODS Injecting ovalbumin（OVA） to sensitize, inhaling OVA to stimulate, and using thyroxin during late stimulation, the asthmatic mouse with Yin deficiency syndrome was established and evaluated through asthmatic behaviors, IL-4 and IL-13 in serum and broncho-alveolar lavage fluid（BALF）, inflammatory cells in BALF and lung tissue, and GATA-3 expression in lung tissue. RESULTS Angelicae Sinensis Radix could reduce asthmatic behaviors, depress the number of inflammatory cells in BALF and lung tissue, IL-4 and IL-13 in serum and BALF, inhibit GATA-3 expression in lung tissue（P〈0.05 or 0.01）. In addition, there were some synergy between Angelicae Sinensis Radix and DXM on eosinophilic cell, IL-4 and GATA-3（P〈0.05 or 0.01）. CONCLUSION Angelicae Sinensis Radix has anti-asthma effect and one of mechanisms may be inhibiting Th2 dominant immune response through depressing expressions of IL-4, IL-13 and GATA-3.